Previous studies with IL-17 deficient mice have reported that IL17A is necessary for the development for AHR or airway inflammation in an OVA-induced asthma model, while administration of exogenous IL-17A in OVA-sensitized C57BL/6J mice reduced the levels of RANTES, CCL17 and Eotaxin-1, improving lung function and reduce levels of eosinophils and lymphocytes in the BALF [22], [29]. This evidence concerns the gene CCL17 and asthma.